|Year : 2021 | Volume
| Issue : 3 | Page : 162-165
Acute severe necrotizing pancreatitis: A manifestation of multisystem inflammatory syndrome in children?
Sailen Kumar Bana, Shivani Deswal, Neelam Mohan
Department of Pediatric Gastroenterology, Hepatology and Liver Transplantation, Medanta – The Medicity Hospital, Gurgaon, Haryana, India
|Date of Submission||12-Jun-2021|
|Date of Decision||05-Aug-2021|
|Date of Acceptance||09-Aug-2021|
|Date of Web Publication||31-Aug-2021|
Dr. Neelam Mohan
Department of Pediatric Gastroenterology, Hepatology and Liver Transplantation, Medanta – The Medicity Hospital, Sector - 38, Gurgaon, Haryana
Source of Support: None, Conflict of Interest: None
Background: Multisystem inflammatory syndrome in children (MIS-C) is commonly being diagnosed among children, 2–8 weeks following a severe acute respiratory syndrome (SARS)-CoV-2 infection. Several cases of pancreatitis have been reported with SARS-CoV-2 infection in adults but only one in a 10-year-old girl with MIS-C. Clinical Description: During the coronavirus disease (COVID) pandemic, a 1-year-old girl presented with high-grade fever for 3 days and vomiting and abdominal pain for a day. Her parents had contracted SARS COVID-2 infection 5 weeks earlier. At admission, she was febrile, drowsy, had tachycardia, tachypnea, and hypotension. Salient examination findings included bilateral nonpurulent conjunctivitis, diminished air entry and crepitation's in the left basal zone, distended abdomen with guarding and tenderness in the left hypochondrium and epigastrium. The diagnostic criteria of MIS-C were fulfilled, but not for classical or incomplete Kawasaki disease. Biochemical markers and radiological findings confirmed acute severe necrotizing pancreatitis. No other etiological cause of pancreatitis could be identified. Management: Intravenous immunoglobulins were started as per protocol. Steroids were withheld in view of the pancreatitis. The child showed dramatic resolution in fever and rapid improvement in clinical and biochemical parameters. Conclusion: Pancreatitis may be a presentation of MIS-C, either due to a direct cytopathic effect or secondary to a hyper-inflammatory response. A high index of suspicion should be kept in children with fever and severe pain abdomen with recent history of COVID-19 infection in the patient or close contacts.
Keywords: Abdominal pain, COVID-19, inflammatory syndrome, pancreas
|How to cite this article:|
Bana SK, Deswal S, Mohan N. Acute severe necrotizing pancreatitis: A manifestation of multisystem inflammatory syndrome in children?. Indian Pediatr Case Rep 2021;1:162-5
|How to cite this URL:|
Bana SK, Deswal S, Mohan N. Acute severe necrotizing pancreatitis: A manifestation of multisystem inflammatory syndrome in children?. Indian Pediatr Case Rep [serial online] 2021 [cited 2021 Sep 26];1:162-5. Available from: http://www.ipcares.org/text.asp?2021/1/3/162/325086
Acute pancreatitis in infants and young children is usually attributable to viral or idiopathic causes. Coronavirus disease 2019 (COVID-19) has been reported to cause pancreatic injury in 8.5%–17.3% of adults with severe acute respiratory syndrome (SARS) CoV-2 infection. Since the angiotensin-converting enzyme 2 (ACE-2) receptors are high in the pancreas, it is plausible to believe that CoV-2 infection can be a potential cause of acute pancreatitis in children as well. A few case reports from the west have described pancreatic involvement in children with acute COVID infection.,, A single case report of COVID-19 associated multisystem inflammatory syndrome in children (MIS-C) presenting as pancreatitis was found on an extensive scientific literature search. However, whether acute pancreatitis can be considered, a presentation of MIS-C is still uncertain.
We report the case of a young child who presented with an acute febrile illness with prominent gastrointestinal (GI) symptoms and who was diagnosed with MIS-C and acute necrotizing pancreatitis. Management was customized accordingly.
| Clinical Description|| |
A 14-month-old girl child presented to the emergency department of our hospital during the second wave of the COVID pandemic in May 2021. She had a history of high-grade fever for 3 days. During this period, she had become lethargic, and her oral intake had progressively decreased. This was followed by multiple episodes of nonbilious vomiting for 1 day. She had episodes of crying, which her parents perceived to be due to abdominal pain. There was no history of loose motions, intake of any meals from external sources, drug intake, yellowish discoloration of the eyes, rashes, or seizures. The frequency of passage of urine was unaffected. There was a significant past history of her parents having developed fever with upper respiratory symptoms 5 weeks earlier and testing positive for SARS CoV-2 by reverse transcription-polymerase chain reaction (RT-PCR) test. Around the same time, the child had also developed fever and loose stools for 2 days for which she was symptomatically treated and recovered. The child was developmentally normal and immunized for age.
At admission, the patient was febrile (38.5 C), had tachycardia (heart rate160/min), tachypnea (respiratory rate45/min) with hypotension (blood pressure 60/40 mmHg, <5th centile for age, sex, and height), SpO2 of 96% in room air. Her weight and length were 9.8 kg and 78 cm, respectively (between 50th and 75th centile). General physical examination revealed some pallor and bilateral nonpurulent conjunctivitis. There was no icterus, clubbing, lymphadenopathy, or rash. The oral cavity was normal. Salient findings on systemic examination included diminished air entry in the left basal zone with crepitations; normal heart sounds with no audible murmur; and a mildly distended abdomen with guarding and tenderness in the left hypochondrium and epigastric region, hepatomegaly (4 cm below the right costal margin in the mid clavicular line with a span was 8.5 cm), and normal bowel sounds. The Glasgow Coma scale was 12/15 (E4, V4, M4). There was no evidence of any cranial nerve involvement, focal neurological deficit, or meningeal irritation. Details of laboratory parameters are depicted in [Box 1].
In the setting of a COVID pandemic, the onset of an acute febrile illness associated with GI symptoms (pain abdomen and vomiting), history of past COVID like illness and positive contact with COVID-infected individuals, nonpurulent conjunctivitis, hypotension, and a tender abdomen was highly suggestive of the possibility of MIS-C. Other differentials that were considered were dengue shock syndrome, scrub typhus, acute pancreatitis, and incomplete Kawasaki disease (KD). Investigations were planned accordingly.
Management and outcome
The child was managed with intravenous fluid as per standard protocol. She was evaluated by rapid COVID RT-PCR test which was negative, after which she was shifted to the intensive care unit. Box 1 lists the reports of the preliminary laboratory investigations. Blood cultures were sterile. NS1 and viral serology were negative for Dengue. Confirmatory tests for malaria and scrub typhus were negative. An abdominal ultrasound revealed an acute edematous pancreatitis with early necrosis in the anterior body of the pancreas with peripancreatic fluid collection, moderate ascites, and bilateral pleural effusion. A computerized tomography (CT) scan confirmed acute necrotizing pancreatitis, peripancreatic inflammation, and an enlarged pancreas showing intraparenchymal necrosis (up to 40%) with a modified CT severity index of up to 10 [Figure 1]. Mild bilateral pleural effusion with underlying areas of atelectasis and patchy consolidation of the left lung base were noted. The viral serology panel for the common causes of acute pancreatitis (cytomegalovirus, coxsackievirus, adenovirus, measles, and rubella) was negative. It was important to rule out KD, especially due to the presence of bilateral nonpurulent conjunctivitis. The echocardiogram demonstrated normal heart chambers, valves, biventricular function, coronaries, and related indices. There was no pericardial effusion. Since the clinical and laboratory profile satisfied the World Health Organization criteria [Table 1], MIS-C with severe pancreatic necrosis was kept as the final diagnosis. The diagnostic criteria for KD and incomplete KD [Table 2] were not fulfilled.
|Table 1: Satisfaction of the World Health Organization criteria of multisystem inflammatory syndrome in children-C in the patient|
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|Table 2: American heart association criteria for incomplete Kawasaki disease and our patient profile (criteria not fulfilled)|
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|Figure 1: Axial contrast abdomen depicting intrapancreatic necrosis in body and tail region (yellow arrowhead)|
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As per standard protocol, intravenous immunoglobulin (IVIG) was given at 2 gm/kg over 48 h. The child became afebrile within 24 h, with improvement in vital parameters and decline in inflammatory markers (C-reactive protein: 9.3 mg/L, ferritin: 70 ng/ml, NT-Pro-BNP66 pg/ml, and lactate dehydrogenase: 371 U/L, lipase: 373 U/L). Clear liquids were started followed by fat-free diet on the 3rd day, which was well tolerated. Prophylactic low molecular weight heparin was started, and aspirin added subsequently in view of thrombocytosis. She was discharged on the 10th day, with no peripancreatic collection or complications. Postillness follow-up remained uneventful with documentation of a normal echocardiography repeated at 2 weeks.
| Discussion|| |
Ever since the pandemic began, there has been extensive research on the effect of COVID-19 on various organ systems, with documentation of evolving evidence of their involvement. The expression of ACE-2 receptors is very high in the endocrine part of the pancreas, in comparison to the exocrine pancreas. Pancreatic injury due to the coronavirus has been attributed primarily due to direct invasion and consequent cytopathic effect. However, other mechanisms of pancreatic injury have also been proposed like systemic inflammatory response or ischemia. A few case reports have described acute pancreatitis as the presenting feature of COVID-19 infection in children., A recent study of 8159 hospitalized children in New York found a significant difference in the incidence of acute pancreatitis in children with COVID-19 (1.8%), in contrast to those who were not infected (0.14).
It has been postulated that viral particles may remain within the GI tract for a long time after the initial COVID-19 infection. In MIS-C, increased mucosal permeability of the gut allows these SARS–CoV-2 antigens to leak into the bloodstream, triggering a cytokine storm and hyperinflammatory response. This could trigger acute pancreatic injury, similar to that described in KD. It is well established that KD and atypical KD like syndrome is seen quite frequently in children infected with SARS-CoV-2 virus.,
Our patient had acute severe necrotizing pancreatitis, the diagnosis of which was established based on clinical, biochemical, and radiological grounds. One may argue that in the setting of a pandemic, most pediatric patients will have SARS CoV-2 immunoglobulin G antibodies, however, our patient also satisfied the diagnostic criteria of MIS-C. Another interesting aspect that was noted was that fever is not the usual presenting symptom of acute pancreatitis. It usually occurs a few days afterward secondary to the inflammatory process. In this case, fever was the initial symptom, and the other common viral causes of acute pancreatitis were negative. We preferred to use IVIG over high-dose steroids due in our case as steroids may aggravate and complicate the severe necrotizing pancreatitis. We believe that this case supports the theory that acute pancreatitis could be a manifestation of MIS-C that may rapidly progress to severe pancreatitis as seen in KD unless appropriate intervention to control the cytokine storm is not initiated in time. Treating pediatricians should keep a high index of suspicion of pancreatitis in children with fever and acute abdomen, especially when associated with a temporal history of COVID infection in the household.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2]